Lipomatous Metaplasia Facilitates Ventricular Tachycardia in Patients With Nonischemic Cardiomyopathy

Ventricular tachycardia (VT) substrate in patients with nonischemic cardiomyopathy (NICM) is complex in distribution and intramural location.

This study sought to test the hypothesis that myocardial lipomatous metaplasia (LM) is a vital anatomic substrate for VT corridors in patients with NICM and VT, and that LM stabilizes current propagation in VT corridors.

Among 49 patients with NICM in the 2-center INFINITY (Prospective Intra-Myocardial Fat Deposition and Ventricular Tachycardia in Cardiomyopathy) Study, potential VT viable corridors within the myocardial scar and/or LM were computed from late gadolinium enhancement cardiac magnetic resonance images and were registered with electroanatomical maps. Corridors passing through VT entrance, isthmus, and/or exit sites, estimated by entrainment or pace mapping, were defined as VT corridors. LM was separately distinguished from scar using computed tomography. The SD of current amplitude along each corridor was measured.

Compared with 151 non-VT corridors, 35 VT corridors traversed a substantially higher volume of LM, with a median 236.6 mg (IQR: 13.5-903.4 mg) vs 5.8 mg (IQR: 0.0-57.9 mg) (P < 0.001). Among corridors with computable current amplitude, 28 VT corridors exhibited substantially lower current variation along the corridors, with SD 8.0 μA (25th-75th percentile: 6.1-10.3 μA) vs 14.9 μA (25th-75th percentile: 8.5-23.7 μA) among 71 non-VT corridors (P < 0.001). Individual VT circuit sites (95 out 118) were highly colocalized with LM.

VT circuitry corridors in NICM are more likely to traverse LM and exhibit reduced current amplitude variation compared with bystander corridors.